One of the main clinical problems associated with stroke recovery is spastic muscle "hypertonia," defined as an abnormal increase in muscle tone. However, despite intensive investigation, the nature, origin and natural history of the mechanical changes in muscle and related soft tissues associated with hypertonia are unknown, due largely to a lack of accurate and sensitive tools for separating the various mechanical contributions to net torque at the spastic joint. Accordingly, as the broad objective of this study, we have developed a novel system identification technique, called parallel cascade identification to address these deficits. This study is designed to demonstrate the feasibility of this technique in quantifying the contributions of intrinsic, passive and reflex mechanical properties to spastic hypertonia and in establishing the natural history of these contributions. Our study will also generate data to assess the feasibility of our novel technique for diagnostic and therapeutic applications. The specific aims are: (1) to characterize the relative contributions of intrinsic, passive and reflex mechanical properties to spastic hypertonia in the stroke elbow, (2) to examine operating point dependencies of these mechanical abnormalities: i.e. variation with joint position, voluntary contraction, and perturbation velocity at each time measured, (3) to explore the time course of mechanical abnormalities in spastic joints following stroke, and (4) to determine the correlation of mechanical abnormalities of spastic limbs with clinical assessment of spasticity and recovery of function. To address the specific aims, a series of perturbation sequences with small amplitudes will be applied to the elbow, and the resulting torque and position signals will be used by a parallel cascade system identification technique to characterize the various contributions to overall joint stiffness. The experiment will be carried out at 1, 3, 6 and 12 months after stroke. The contralateral side will be tested as control. The correlation between the results obtained by this technique with other clinical measures of the severity of spasticity and recovery of function will also be measured. We expect that the reflex contributions to mechanical abnormalities associated with spastic hypertonia increase within weeks of stroke and remain high. This hyperexcitability may lead progressively to shortening of fiber length in spastic muscle and to changes in the neutral position of the spastic joint. Persistent positional deformity and the accumulation of connective tissues in atrophic muscles secondary to the lesions may increase the passive contribution to joint torque continuously with time, but decrease intrinsic muscle contributions. The changes in passive and intrinsic stiffness are likely to be highly correlated with severity of spasticity and inversely correlated with recovery of function.